Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Systems Exam 1 > Hematopathology I: RBC > Flashcards

Hematopathology I: RBC Flashcards

(49 cards)

Start Studying
1
Q

what is Anemia?

A

a reduction in the oxygen carrying capacity of the blood and reduction of the total circulating red cell mass of RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What triggers erythropoietin secretion by renal cells and what does it lead to?

A

decrease in tissue oxygen, leading to:
- Hyperplasia of erythroid precursors in the bone marrow
- Extramedullary hematopoiesis in severe cases
- Reticulocytosis: release of immature red cells into circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is anemia diagnosed in lab investigations?

A
  • Peripheral blood smear: Assesses RBC morphology
  • RBC size: Normocytic, microcytic, or macrocytic
  • RBC color: Normochromic or hypochromic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the normal RBC values when evaluating in a lab?

A
  • RBC count: M 4.9 ; F 4.4
  • Hemoglobin: M 16 ; F 14
  • Hematocrit: M 47 ; F 42
  • Mean Cell: M 34 ; F 34
  • Mean Cell Volume: M 95 ; F 95
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the three major causes of anemia?

A
  • bleeding (most common)
  • hemolysis
  • diminished erythropoiesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the common symptoms of anemia?

A

pallor
fatigue
lassitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is blood loss anemia categorized (hemorrhagic anemia)?

A
  • Acute
  • Chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are key features of acute blood loss anemia?

A
  • shock from severe hemorrhage that results in normocytic, normochromic anemia
  • Replacement begins quickly if iron stores are adequate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are key features of chronic blood loss anemia?

A

GI ulcers, IBS, irregular menstrale cycles causes ongoing blood loss which leads to gradual iron depletion resulting in microcytic, hypochromic anemia over time (iron deficiency anemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a complication of ineffective red blood cell (RBC) production over time?

A

Iron overload, which may result from repeated transfusions or chronic ineffective erythropoiesis (RBCs do not mature properly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What defines hemolytic anemia?

A

Shortened lifespan of RBCs (normal = 120 days) due to inherent RBC defect or acquired disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the key featurees of hemolytic anemia?

A
  • ↑ RBC destruction → low RBC count
  • ↑ Erythropoiesis → more reticulocytes in blood
  • Breakdown of heme → ↑ bilirubin (Hyperbilirubinemia) → jaundice and pigmented gallstones
  • Bone marrow expands; extramedullary hematopoiesis may occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is hereditary spherocytosis, and what causes it?

A
  • genetic disorder (mostly autosomal dominant) caused by mutations in proteins like ankyrin, spectrin, band 3, and band 4.2, which form the RBC cytoskeleton which leads to loss of membrane integrity and formation of spherical RBCs (spherocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do spherocytes contribute to anemia in hereditary spherocytosis?

A

Spherocytes are less deformable and get trapped and destroyed in the spleen by macrophages, leading to extravascular hemolysis, anemia, and splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the treatment for hereditary spherocytosis?

A

Splenectomy (removes site of RBC destruction, improves anemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes Sickle Cell Anemia?

A

A mutation in the β-globin gene where glutamic acid is replaced by valine at position 6 of the β chain which creates abnormal Hemoglobin S (HbS).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do homozygous and heterozygous states differ in sickle cell anemia?

A
  • Homozygotes (HbS/HbS): Have sickle cell anemia
  • Heterozygotes (HbS/HbA): Have sickle cell trait (asymptomatic carriers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the consequences of sickled cells in the body?

A
  • sickled cells are removed by splenic macrophages → hemolytic anemia (RBC lifespan ~20 days).
  • leads to expanded erythropoiesis → “hair-on-end” skull X-rays
  • Microvascular occlusion → painful crises, autosplenectomy, stroke, and lung infarcts.
  • low oxygen areas (spleen, bone marrow, inflammation) increase sickling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do other hemoglobins affect sickling severity?

A
  • HbA inhibits HbS polymerization → milder symptoms in trait
  • HbC enhances polymerization with HbS → more symptoms
  • HbF reduces sickling; symptoms begin after 4-5 months when HbF declines.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Thalassemia and what are its major types?

Study These Flashcards
A

a group of genetic disorders with decreased synthesis of globin chains in hemoglobin
- β-Thalassemia: Mutations in β-globin gene
- α-Thalassemia: Deletions in α-globin genes

21
Q

What are the differences between β-Thalassemia minor and major?

Study These Flashcards
A
  • β-Thalassemia minor (one abnormal β allele): Mild/no symptoms, microcytic hypochromic anemia
  • β-Thalassemia major (two abnormal β alleles): Severe anemia, requires transfusions, develops when HbF declines
22
Q

What is the pathophysiology of β-Thalassemia major?

Study These Flashcards
A
  • Decreased β-globin → excess α-globin → aggregates → RBC damage and removal by spleen
  • leads to ineffective erythropoiesis, bone marrow expansion, and skeletal deformities
    **Iron overload from transfusions → treat with iron chelators
23
Q

What are the effects of different deletions in α-Thalassemia?

Study These Flashcards
A
  • 1 deletion: Silent carrier
  • 2 deletions: α-thalassemia trait (mild symptoms)
  • 3 deletions: HbH disease (β4 tetramers) → binds O₂ too tightly
  • 4 deletions: Hydrops fetalis (lethal)
24
Q

What happens in G6PD deficiency and what does it cause?

Study These Flashcards
A

Low G6PD → less NADPH → less GSH → oxidants build up which causes oxidative damage to hemoglobin (Hb):
- Denaturing (loses shape)
- Precipitates (clumps inside RBCs)

*Damaged RBCs break apart → hemolytic anemia

25
who is most affected by G6PD Deficiencies?
Inherited on X chromosome → mostly affects males
26
When do symptoms of G6PD deficiency appear and how is it reversed?
- No symptoms unless exposed to oxidative stress from certain drugs, bacterial toxins, infections, or free radicals - acute and reversible as new RBCs with working enzyme are made
27
What is the main cause of immunohemolytic anemia?
Antibodies bind to RBCs—either normal or altered—marking them for destruction - can be due to autoimmune diseases or drugs/chemicals acting as haptens
28
What does the Coombs test detect?
checks for anti-RBC antibodies that are either: - bound to RBCs (direct Coombs test) - free-floating in the blood (indirect Coombs test)
29
What roles do IgG and IgM antibodies play in RBC destruction?
- IgG coats RBCs, leading to phagocytosis by macrophages (mainly in the spleen) - IgM activates complement, causing intravascular hemolysis or opsonization by C3b
30
Is immunohemolytic anemia always severe?
No—severity varies - Most cases are mild and chronic, but it can occasionally be more acute or severe.
31
What is the main cause of Hemolytic anemia due to mechanical trauma?
disseminated intravascular coagulation causing damage to vessel walls or formation of fibrin clots leading to obstructed narrowed blood vessels
32
What happens when merozoites from Malaria lifecycle burst out of RBCs?
cyclic fevers, chills, and shaking every 48–72 hours which leads to hemolysis, and can cause: - Hemoglobinemia, jaundice, hemoglobinuria ("blackwater fever") - Splenomegaly as the spleen removes damaged RBCs.
33
How does malaria affect the brain?
Parasitized RBCs clump together, blocking small brain vessels which causes microthrombi, leading to: - Brain damage, seizures, coma, or even death
34
what are the anemias of diminished erythropoisis?
- Iron Deficiency Anemia - Megaloblastic Anemia - Aplastic Anemia - Myelophthisic Anemia
35
what are the causes of iron deficiency anemia?
- Low iron intake - Poor absorption - Increased need for iron (pregnancy, infancy, or rapid growth) - Chronic blood loss
36
how does iron deficiency anemia develop and what are the effects on the bone marrow?
slowly overtime, you make less hemoglobin, myoglobin, and other iron-containing proteins that leads to hypochromic, microcytic anemia and bone marrow hyperplasia
37
what are the common symptoms of iron deficiency anemia?
Fatigue Weakness Pallor (pale skin) Atrophic glossitis (smooth, sore tongue)
38
What causes Anemia of Chronic Disease?
chronic inflammation (e.g. osteomyelitis, endocarditis, Crohn’s, RA, Hodgkin lymphoma) that leads to: - IL-1/TNF mediated iron sequestration in macrophages (iron trapped, not available for red blood cell production)
39
What causes megaloblastic anemia?
Deficiency in folate or vitamin B₁₂, both needed for DNA synthesis during red blood cell production.
40
What is the result of impaired DNA synthesis in megaloblastic anemia?
- Delayed nuclear maturation and cell division - Enlarged RBC precursors (megaloblasts) and macrocytic RBCs - Hypersegmented neutrophils. - Pancytopenia due to decreased cell output
41
What are common symptoms of folate or B₁₂ deficiency?
Slow turnover of gastrointestinal cells → sore tongue (glossitis), cheilosis. - In vitamin B₁₂ deficiency: demyelinating neuropathy of spinal cord and peripheral nerves
42
What is pernicious anemia?
A form of vitamin B₁₂ deficiency due to lack of intrinsic factor caused by: - Autoantibodies against parietal cells or intrinsic factor - Gastric atrophy or gastrectomy - Resection of distal ileum or malabsorption syndromes (e.g., Crohn's).
43
What is aplastic anemia?
A bone marrow failure syndrome due to suppression of multipotent myeloid stem cells, leading to pancytopenia (anemia, thrombocytopenia, neutropenia)
44
What causes aplastic anemia?
- Mostly idiopathic - Can be triggered by myelotoxic drugs, radiation, or viral infections - May involve T-cell–mediated destruction of stem cells
45
What are the clinical features of aplastic anemia?
- Symptoms of anemia (fatigue, pallor) - Bleeding (petechiae, ecchymoses) due to low platelets - Recurrent infections due to neutropenia
46
Why is the progression of aplastic anemia unpredictable?
Causes can be temporary or persistent - May resolve by stopping a drug or require bone marrow transplant
47
What is the immunologic mechanism involved in aplastic anemia?
- Environmental insults cause genetic alterations in stem cells and express new antigens - T cells produce IFNγ and TNF → suppress marrow → marrow aplasia
48
What is Myelophthisic Anemia and what causes it?
occurs when the bone marrow is extensively replaced or infiltrated by abnormal substances and crowd out healthy blood-forming (hematopoietic) cells, impairing the marrow’s ability to produce blood cells - causes: fibrosis (scar tissue), tumor cells (e.g., metastatic cancer, leukemia, multiple myeloma), infections (e.g., tuberculosis) and bone disorders (e.g., osteosclerosis)
49
What are the symptoms of Myelophthisic Anemia?
- Anemia (fatigue, pallor, weakness) due to low red blood cell production - Thrombocytopenia (easy bruising, bleeding) due to reduced platelet formation

Systems Exam 1 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions